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Biomedical subjects

C R Walker

Publications and source records attributed to C R Walker.

11 recordsLinked to original sources

Dexamethasone therapy for bronchopulmonary dysplasia: improved respiratory mechanics without adrenal suppression.

The purpose of the present study was to examine the pattern of changes in respiratory system mechanics induced by dexamethasone (Dex) in infants with bronchopulmonary dysplasia (BPD) and to determine whether dosages that produce these changes induce adrenal suppression. We examined mechanics in seven ventilator-dependent premature infants (age, 33 +/- 4.8 days) with BPD, before and daily during Dex therapy. Dex (0.5 mg/kg/day) was given intravenously for 7 days unless complications necessitated early termination. Respiratory system resistance (Rrs) and compliance (Crs) were measured by the passive expiratory flow-volume technique during the course of dexamethasone therapy or until extubation. Adrenocorticotrophic hormone (ACTH) stimulation tests were done at baseline and following Dex therapy to evaluate adrenal function. Dex therapy caused a 77 +/- 18% increase in Crs (from 0.97 +/- 0.09 SEM mL/cmH2O to 1.6 +/- 0.16 mL/cmH2O; P less than 0.025) and a 33 +/- 5% decrease in Rrs (from 0.20 +/- 0.02 cmH2O/mL/s to 0.14 +/- 0.01 cmH2O/mL/s; P less than 0.01). Concurrently, ventilator rate, mean airway pressure, and FIO2 all decreased significantly (P less than 0.025). Extubation occurred later in infants with the lowest Crs and highest Rrs at baseline. At extubation, all Crs values were greater than 1.33 mL/cmH2O and Rrs values were less than 0.15 cmH2O/mL/s. Systolic blood pressure increased from 61 +/- 6.3 mmHg to 84 +/- 17 mmHg, 72-96 h after the start of Dex (P less than 0.025). There were no episodes of culture-positive sepsis. Neither basal nor ACTH-stimulated levels of cortisol were suppressed as a result of Dex therapy (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands

Colon cancer in blacks: a disease with a worsening prognosis.

Despite the fact that a significant national effort has been made over the past 10 years to improve the early detection and treatment of colorectal cancer, blacks have not had any change in their prognosis compared to whites, and their survival rate appears to be independent of stage at the time of diagnosis. The disease incidence is practically the same for both races, 49 per 100,000. We reviewed all patients with colorectal cancer in our Tumor Registry over a 10-year period to determine whether the experience at an all-black institution with a black patient base for much of its history would help clarify these crucial questions. There were 118 cases (73 women/45 men), and the mean age was 68 years (range: 29 to 93). The most common signs and symptoms were gross bleeding (34%) and abdominal pain (30%), with most patients presenting with a combination of symptoms. Remarkably, none were symptom-free. Of the 96 patients who were staged surgically and pathologically, 68 (71%) were beyond Duke's B staging at the time of diagnosis and surgery. The overall 5-year survival rate was 47%, significantly related to stage of disease at diagnosis (P less than .001). We concluded that blacks have not shared in the progress made in early diagnosis and treatment of colon cancer, and that special attention should be given to developing screening and surveillance methodology targeted specifically at blacks.

Adenocarcinoma

Diazepam inhibits myoblast fusion and expression of muscle specific protein synthesis.

The presence of diazepam in culutres of chicken embryo myoblasts arrests normal muscle cell differentiation. High concentrations of the drug reversibly prevent myoblasts from fusing to form multinucleated myotubes. Lower concentrations of diazepam allow cell fusion to occur, but inhibit the synthesis and accumulation of myosin heavy chain, implying that cell fusion does not obligate myoblasts to synthesize and accumulate large quantities of muscle specific protein. The effect of diazepam on muscle cells in culture is direct and specific.

Animals

Regulation of newly synthesized acetylcholinesterase in muscle cultures treated with diisopropylfluorophosphate.

Brief treatment with 0.1 mM diisopropylfluorophosphate inhibited an average of 89% of the acetylcholinesterase (EC 3.1.1.7; acetylcholine hydrolase) activity of cultures of chick embryo muscle. As long as protein synthesis occurred, an average of 78% of the activity returned within 4 hr. Newly synthesized acetylcholinesterase did not stain cytochemically, was rapidly and extensively degraded or released in the presence of 10 muM cycloheximide, and consisted mainly of low-molecular-weight forms. Acetylcholinesterase activity first appeared around the nucleus, about 4 hr after treatment with diisopropylfluorophosphate, and then spread to the rest of the cell about the time release of acetylcholinesterase was detected in the medium. With time, more and more of the enzyme was retained in the cells after treatment with cycloheximide, and the proportions of low-molecular-weight forms decreased and high-molecular-weight forms increased. The results suggest that newly synthesized acetylcholinesterase undergoes an orderly process of binding, movement, and assembly in diisopropylfluorophosphate treated, and probably also in untreated, embryo muscle fibers.

Acetylcholinesterase